Immunoglobulin E (IgE) and mast cells play important roles in the pathogenesis of allergic asthma. Catalpol, an iridoid glycoside, exerts many biological functions including anti-inflammatory activities. Herein, we investigated catalpol to determine both its antiallergic effects on IgE/ovalbumin (OVA)-stimulated mouse bone marrow-derived mast cells and its therapeutic actions in murine allergic asthma. We found that catalpol dramatically suppressed IgE/OVA-induced mast cell degranulation. Meanwhile, 5 ~ 100 μM of catalpol neither affected the expression level of the high-affinity receptor of IgE (FcεRI) by mast cells nor induced mast cell apoptosis. In addition, mRNA expression levels of inflammatory enzymes including cyclooxygenase (COX)-1, COX-2, and 5-lipoxygenase were downregulated. Administration of catalpol also suppressed production of prostaglandin D (PGD), interleukin (IL)-6, and IL-13, while not affecting tumor necrosis factor (TNF)-α production. Further, catalpol pretreatment significantly attenuated the FcεRI-mediated Akt signaling pathway. In mice with IgE/OVA-induced asthma, oral administration of catalpol remarkably suppressed the production of OVA-specific IgE, the development of airway hyperresponsiveness (AHR), and the infiltration of eosinophils and neutrophils into the lungs. Histological studies demonstrated that catalpol substantially inhibited the recruitment of mast cells and increased mucus production in lung tissues. Catalpol-treated mice had significantly lower levels of helper T cell type 2 (Th2) cytokines (IL-4, IL-5, and IL-13), PGD, eotaxin-1, and C-X-C chemokine ligand-1 (CXCL1) in bronchoalveolar lavage fluid (BALF) than did the allergic group. Collectively, these results indicated that the suppressive effects of catalpol on degranulation and mediator generation by mast cells were beneficial in treating allergic asthma.
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